Obesity is typically accompanied by hyperisulinemia which contributes to metabolic efficiency and perpetuates the obese state. As obesity is a significant risk factor for the development of Type II diabetes, understanding the factors contributing to the hyperinsulinemia associated with obesity are of significant clinical concern. Many animal models of obesity exhibit hyperinsulinemia that can be attenuated by vagotomy or administration of atropine, suggesting mediation by the vagus nerve. Furthermore, animal work demonstrates that increases in vagal efferent activity can occur following over-stimulation of the B-cell. The hypothesis of this study is that increased vagal efferent activity potentiates the hyperinsulinemia of human obesity. The objective of this study is to determine if the hyperinsulinemia induced by over-stimulation of the B-cell is mediated by an increase in vagal eefferent activity. Insulin sensitivity using a frequently sampled intravenous glucose tolerance test will be measured prior to and following a 48-h infusion of glucose in the presence and absence of atropine.